1. PHYSIOLOGY OF EAR
The Nature of Sound Waves:
Sound waves are alternating high and low pressure regions traveling in a direction
through some medium (such as air) like ripples arise and travel over the surface of a pond
while tossing a stone into it.
The frequency of a sound vibration is its pitch.
The higher the frequency of vibration, the higher is the pitch.
The sounds heard most acutely by the human ear are at frequencies between 500 and
5000 hertz (Hz).
1 Hz = 1 cycle per second.
The entire audible range extends from 20 to 20,000 Hz. Sounds of speech primarily
contain frequencies between 100 and 3000 Hz, and the “high C” sung by a soprano
has a dominant frequency at 1048 Hz.
The larger the intensity (size or amplitude) of the vibration, the louder is the sound.
Sound intensity is measured in units called decibels (dB).
An increase of one decibel represents a tenfold increase in sound intensity. The
hearing threshold-the point at which an average young adult can just distinguish
sound from silence is defined as 0 dB at 1000 Hz.
Whispered speech has a decibel level of 30; normal conversation, 60; shouting, 80;
and a nearby motorcycle, 90. Sound becomes uncomfortable to a normal ear at about
120 dB, and painful above 140 dB. Rock concerts and headphones can easily produce
sounds over 110 dB.
Continued exposure to high-intensity sounds is a cause of deafness or total hearing
loss. Deafness usually begins with loss of sensitivity for high-pitched sounds.
Most people fail to notice their progressive hearing loss until destruction is extensive
and they begin having difficulty understanding speech. Wearing earplugs with a
noise-reduction rating of 30 dB can protect the sensitivity of ears.
2. PHYSIOLOGY OF HEARING:
The events involved in hearing are:
1. The auricle directs sound waves into the external auditory canal. When sound waves
strike the tympanic membrane, the vibrations causes the tympanic membrane to
vibrate back and forth.
2. The distance moved depends on the intensity and frequency of the sound waves
(eardrum vibrates slowly to low-frequency/low-pitched sounds and rapidly to high-
frequency/high-pitched sounds).
3. The central area of the eardrum connected to the malleus starts to vibrate and
vibration is transmitted to incus and to the stapes. The stapes moves back and forth,
and pushes the membrane of the oval window in and out.
4. The oval window vibrates about 20 times more vigorously than the eardrum because
the ossicles efficiently transmit small vibrations spread over a large surface area
(eardrum) into larger vibrations of a smaller surface (oval window).
5. The movement of the oval window sets up fluid pressure waves in the perilymph of
the cochlea. As the oval window bulges inward, it pushes on the perilymph of the
scala vestibuli.
6. Pressure waves are transmitted from the scala vestibuli to the scala tympani and
eventually to the round window, causing it to bulge outward into the middle ear.
7. As the pressure waves deform the walls of the scala vestibuli and scala tympani, they
also push the vestibular membrane back and forth, creating pressure waves in the
endolymph inside the cochlear duct.
8. The pressure waves in the endolymph cause the basilar membrane to vibrate, which
moves the hair cells of the spiral organ against the tectorial membrane. This leads to
bending of the hair cell stereocilia, which produces receptor potentials that ultimately
lead to the generation of nerve impulses.
3. Sound waves of various frequencies cause regions of the basilar membrane to vibrate
more intensely. Membrane is narrower and stiffer at the base of the cochlea (portion
closer to the oval window), high-frequency (high-pitched) sounds near 20,000 Hz
induce maximum vibrations in this region.
At the apex of the cochlea near the helicotrema, the basilar membrane is wider and
more flexible; low-frequency (low-pitched) sounds near 20 Hz cause maximum
vibration of the basilar membrane in this region.
Loudness is determined by the intensity of sound waves. High-intensity sound waves
cause larger vibrations of the basilar membrane, which leads to a higher frequency of
nerve impulses reaching the brain. The hair cells transduce mechanical vibrations into
electrical signals.
A tip link protein connects the tip of each stereocilium to a mechanically gated ion
channel called the transduction channel. As the stereocilia bend in the direction of
the taller stereocilia, the tip links tug on the transduction channels and open them.
These channels allow cations in the endolymph, primarily K+, to enter the hair cell
cytosol. As cations enter, they produce a depolarizing receptor potential.
Depolarization quickly spreads along the plasma membrane and opens voltage-gated
Ca2+ channels in the base of the hair cell.
The resulting inflow of Ca2+ triggers exocytosis of synaptic vesicles containing a
neurotransmitter, glutamate. Neurotransmitter is released, in the sensory neurons that
synapse with the base of the hair cell.
Bending of the stereocilia in the opposite direction closes the transduction channels,
allows hyperpolarization to occur, and reduces neurotransmitter release from the hair
cells.
This decreases the frequency of nerve impulses in the sensory neurons.
The cochlea has the surprising ability to produce inaudible sounds, called otoacoustic
emissions and can be picked up by placing a sensitive microphone next to the
eardrum. They are caused by vibrations of the outer hair cells that occur in response
to sound waves and to signals from motor neurons.
As they depolarize and repolarize, the outer hair cells rapidly shorten and lengthen.
The outer hair cell vibrations set up a traveling wave that goes back toward the stapes
and leaves the ear as an otoacoustic emission.
Detection of these inner ear-produced sounds is a fast, inexpensive, and noninvasive
way to screen newborns for hearing defects.
THE AUDITORY PATHWAY:
Bending of the stereocilia of the hair cells of the spiral organ causes the release of a
neurotransmitter (glutamate), which generates nerve impulses in the sensory neurons
that innervate the hair cells.
4. The cell bodies of the sensory neurons are located in the spiral ganglia. Nerve
impulses pass along stimulate the axons of these neurons, forming the cochlear branch
of the vestibulocochlear (VIII) nerve. These axons synapse with neurons in the
cochlear nuclei in the medulla oblongata on the same side.
Some of the axons from the cochlear nuclei decussate (cross over) in the medulla,
ascend in a tract called the lateral meniscus on the opposite side, and terminate in the
inferior colliculus in the midbrain. Other axons from the cochlear nuclei end in the
superior olivary nucleus in the pons on each side.
Slight differences in the timing of nerve impulses arriving from the two ears at the
superior olivary nuclei allow us to locate the source of a sound.
Axons from the superior olivary nuclei also ascend in the lateral meniscus tracts on
both sides and end in the inferior colliculi.
From each inferior colliculus, nerve impulses are conveyed to the medial geniculate
nucleus in the thalamus and finally to the primary auditory area of the cerebral
cortex in the temporal lobe of the cerebrum.
Because many auditory axons decussate in the medulla while others remain on the
same side, the right and left primary auditory areas receive nerve impulses from both
ears.
PHYSIOLOGY OF EQUILIBRIUM:
There are two types of equilibrium (balance).
Static equilibrium refers to the maintenance of the position of the body (mainly the
head) relative gravity. Body movements of static equilibrium include tilting the head
and linear acceleration or deceleration.
Dynamic equilibrium is the maintenance of body position (mainly the head) in
response to rotational acceleration or deceleration.
The receptor organs for equilibrium are called the vestibular apparatus; these include
the saccule, utricle, and semicircular ducts.
Otolithic Organs: Saccule and Utricle. The walls of both the utricle and the saccule
contain a small, thickened region called a macula. The two maculae (plural), which
5. are perpendicular to one another, are the receptors for static equilibrium. They provide
sensory information on the position of the head in space and are essential for
maintaining appropriate posture and balance.
The maculae also detect linear acceleration and deceleration. The maculae consist of
two kinds of cells: hair cells, which are the sensory receptors, and supporting cells.
Hair cells have stereocilia (microvilli) of graduated height and 1 kinocilium (a cilium
anchored firmly to its basal body and extending beyond the longest stereocilium).
The stereocilia are connected by tip links. The stereocilia and kinocilium forms hair
bundle. The columnar supporting cell secretes the thick, gelatinous, lycoprotein layer,
called the otolithic membrane that rests on the hair cells.
A layer of dense calcium carbonate crystals (otoliths) spread over the entire otolithic
membrane on top of the macula. While tilting the head forward, the otolithic
membrane and the otoliths are pulled by gravity. It slides “downhill” over the hair
cells bending the hair bundles.
As the hair cells depolarize and repolarize, they release neurotransmitter at a faster or
slower rate. The hair cells synapse with sensory neurons in the vestibular branch of
the vestibulocochlear (VIII) nerve. These neurons fire impulses at a slow or rapid rate
depending on the amount of neurotransmitter present.
Motor neurons also synapse with the hair cells and sensory neurons and regulate the
sensitivity of the hair cells and sensory neurons.
Semicircular Ducts: The three semicircular ducts function in dynamic equilibrium.
The ducts lie at right angles to one another in three planes: The two vertical ducts are
the anterior and posterior semicircular ducts, and the horizontal one is the lateral
semicircular duct. This positioning permits detection of rotational acceleration or
deceleration.
In the ampulla, the dilated portion of each duct, is a small elevation called the crista
(plural is cristae). Each crista contains a group of hair cells and supporting cells.
Covering the crista is a mass of gelatinous material called the cupula.
When head moves, the attached semicircular ducts and hair cells move with it. The
endolymph within the ampulla, is not attached and lags behind. As the moving hair
cells drag along the stationary endolymph, the hair bundles bend.
Bending of the hair bundles produces receptor potentials and lead to nerve impulses
that pass along the vestibular branch of the vestibulocochlear (VIII) nerve.
In the ampulla, the dilated portion of each duct, is a small elevation called the crista
(plural is cristae). Each crista contains a group of hair cells and supporting cells.
Covering the crista is a mass of gelatinous material called the cupula.
6. When head moves, the attached semicircular ducts and hair cells move with it. The
endolymph within the ampulla, is not attached and lags behind. As the moving hair
cells drag along the stationary endolymph, the hair bundles bend.
Bending of the hair bundles produces receptor potentials and lead to nerve impulses
that pass along the vestibular branch of the vestibulocochlear (VIII) nerve.
EQUILIBRIUM PATHWAYS:
Bending of hair cells in the semicircular ducts, utricle, or saccule causes the release
of a neurotransmitter (glutamate), which generates nerve impulses in the sensory
neurons that innervate the hair cells.
The cell bodies of sensory neurons are located in the vestibular ganglia. Nerve
impulses pass along the axons of these neurons, which form the vestibular branch of
the vestibulocochlear (VIII) nerve. Most of these axons synapse with sensory neurons
in vestibular nuclei, the major integrating centers for equilibrium, in the medulla
oblongata and pons.
The vestibular nuclei also receive input from the eyes and somatic receptors,
especially proprioceptors in the neck muscles that indicate the position of the head.
The remaining axons enter the cerebellum through the inferior cerebellar peduncles.
Bidirectional pathways connect the cerebellum and vestibular nuclei.
7. The vestibular nuclei integrate information from vestibular visual, and somatic
receptors and then send commands to:
The nuclei of cranial nerves-oculomotor (III), trochlear (IV), and abducens (VI)-that
control coupled movements of the eyes with those of the head to help maintain focus
on the visual field;
Nuclei of the accessory (XI) nerves to help control head and neck movements to assist
in maintaining equilibrium;
The vestibulospinal tract, which conveys impulses down the spinal cord to maintain
muscle tone in skeletal muscles to help maintain equilibrium; and
The ventral posterior nucleus in the thalamus and the vestibular area in the parietal
lobe of the cerebral cortex provide us with the conscious awareness of the position
and movements of the head.
DISEASES OF THE EAR:
1. External otitis:
Staphylococcus aureus is the usual cause of localised inflammation (boils) in the
external auditory meatus.
The inflammation may be caused by bacteria or fungi or by an allergic reaction to
dandruff, soaps, hair sprays, hair dyes etc.
2. Acute otitis media:
It is inflammation of the middle ear cavity caused by spread of microbes from an
upper respiratory tract infection via the auditory tube. Common in children with
severe earache.
8. It may spread from the outer ear through perforation in the tympanic membrane
leading to the accumulation of pus and the outward bulging of the tympanic
membrane.
Sometimes rupture the tympanic membrane and result in purulent discharge from
the ear (otorrhoea) and cause mastoiditis and labyrinthitis.
The petrous portion of the temporal bone is very thin; the infection may spread
causing meningitis and brain abscess.
3. Serous otitis media:
'Glue ear', or secretory otitis media, is the collection of fluid (effusion) in the middle
ear cavity. Causes include:
a) Obstruction of the auditory tube by pharyngeal swelling enlarged adenoids or
tumour.
b) Barotrauma (usually caused by descent in an aeroplane when suffering from a
cold).
c) Untreated acute otitis media.
Adults suffer from deafness and painless blockage of the ear. Children show delay
in speech development and behavioural disorders owing to deafness.
Air present in the middle ear is absorbed and a negative pressure develops
resulting in retraction of the tympanic membrane.
Fluid is drawn into the low-pressure cavity from surrounding blood vessels.
Conductive hearing loss occurs and may lead to secondary infection. (Common
cause for hearing impairment in children).
4. Chronic otitis media:
Permanent perforation of the tympanic membrane due to acute otitis media (with
recurrent, persistent or untreated) and mechanical or blast injuries.
During the healing process stratified epithelium from the outer ear grows into the
middle ear, forming a cholesteatoma (It is a collection of scaling epithelial cells
and pus forming material).
Continued development of cholesteatoma may lead to:
a. Destruction of the ossicles and conduction deafness.
b. Erosion of the roof of the middle ear and meningitis.
c. Spread of infection to the inner ear that may cause labyrinthitis.
5. Otosclerosis:
A common cause of progressive conductive hearing loss in young adults affecting
one ear but is more commonly bilateral.
It is usually hereditary, more common in females than males and often worsens
during pregnancy.
Abnormal bone develops around the footplate of the stapes fusing it to the oval
window, reducing the ability to transmit sound waves across the tympanic cavity.
6. Presbycusis:
This form of hearing impairment commonly accompanies the ageing process.
Degenerative changes in the sensory cells of the spiral organ of Corti resulting in
sensorineural (perceptive) deafness.
9. Perception of high-frequency sound is impaired first and later low-frequency
sound may also be affected.The individual develops difficulty in discrimination,
e.g. following a conversation in the presence of background noise.
7. Meniere's disease:
It is a condition in which accumulation of endolymph cause distension and
increased pressure in the membranous labyrinth with destruction of the sensory
cells in the ampulla and cochlea.
It is usually unilateral but both ears may be affected later. The cause unknown.
Meniere's disease is associated with recurrent episodes of dizziness (vertigo),
nausea and vomiting, lasting for several hours. There may be continuous ringing
in the affected ear (tinnitus).
Permanent hearing impairment develop as the spiral organ of Corti is destroyed.
8. Labyrinthitis:
Caused by development of a fistula from a cholesteatoma or by spread of infection
from the middle ear.
The spiral organ may be destroyed, causing sudden total nerve deafness in the
affected ear.
9. Motion sickness:
Repetitive motion causes excessive stimulation of the semicircular canals and
vestibular apparatus and results in nausea and vomiting in some people.
10. Deafness:
Hearing impairment can be classified in to 2 as conductive and sensorineural and
mixed when there is a combination of both types of deafness in one ear.
a. Conductive deafness:
This is due to impaired transmission of sound waves from the outside to the
oval window, i.e. an abnormality of the outer or middle ear.
b. Sensorineural (perceptive) deafness:
This is due to disease of the cochlea, the cochlear branch of the vestibular
nerve or the hearing area of the brain. The individual perceives noise but
cannot discriminate/understand between sounds.
Risk factors for congenital deafness include:
• Family history of hereditary deafness
• Viruses, e.g. maternal rubella during the first 3 months of pregnancy.
• Acute hypoxia at birth.